title: Occlusion of portosystemic shunts improves hyperinsulinemia due to insulin resistance in cirrhotic patients with portal hypertension.
abstract: BACKGROUND
  Liver cirrhosis (LC) is often complicated by hyperinsulinemia due to insulin resistance (IR), which is considered to be closely related to shunt formation and impaired liver function. This study evaluates whether balloon-occluded retrograde transvenous obliteration (B-RTO) can affect glucose and insulin metabolism in patients with LC.
  
  
  METHODS
  Twenty-five cirrhotic patients (mean age = 69.6 years; female/male = 12/13; hepatitis C virus/alcohol/nonalcoholic steatohepatitis = 14/6/5; Child-Pugh's class A/B = 10/15) with gastric varices and/or hepatic encephalopathy caused by portosystemic shunts (PSS) due to portal hypertension (PH) underwent B-RTO at our hospital. Testing was performed before and at 1 month after the procedure.
  
  
  RESULTS
  Shunt occlusion resulted in a decrease in extrahepatic collateral blood flow and an increase in portal venous flow, as well as a dramatic improvement in hepatic function markers. In addition, B-RTO significantly decreased homeostasis model assessment (HOMA) of IR without a statistical decline of HOMA of β-cell function. The 75-g oral glucose tolerance test (75-OGTT) revealed that occlusion of PSS reduced both fasting immunoreactive insulin (IRI) levels and the area under the curve for IRI. However, no significant change in preprandial or postprandial plasma glucose levels was observed. Furthermore, according to the criteria of the American Diabetes Association, B-RTO led to an improved 75-OGTT profile in 58.3 % of patients who had impaired glucose tolerance or diabetes mellitus before the procedure.
  
  
  CONCLUSIONS
  Shunt occlusion improves IR-related hyperinsulinemia through increased portal venous flow, ameliorated liver function, and consequent augmented hepatic insulin clearance in cirrhotic patients with PH.
authors.affiliation: Department of Gastroenterology and Hepatology, Yamaguchi University Graduate School of Medicine, 1-1-1 Minami-Kogushi, Ube, Yamaguchi, 7558505, Japan, tsu0920@yamaguchi-u.ac.jp.
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Ishikawa
authors.forename: Shogo
authors.initials: S
authors.lastname: Shiratsuki
authors.forename: Takashi
authors.initials: T
authors.lastname: Matsuda
authors.forename: Takuya
authors.initials: T
authors.lastname: Iwamoto
authors.forename: Taro
authors.initials: T
authors.lastname: Takami
authors.forename: Koichi
authors.initials: K
authors.lastname: Uchida
authors.forename: Shuji
authors.initials: S
authors.lastname: Terai
authors.forename: Takahiro
authors.initials: T
authors.lastname: Yamasaki
authors.forename: Isao
authors.initials: I
authors.lastname: Sakaida
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D021721:Balloon Occlusion / Q000379:methods*; D004932:Esophageal and Gastric Varices / Q000209:etiology; D005260:Female; D005947:Glucose / Q000378:metabolism; D005951:Glucose Tolerance Test; D006501:Hepatic Encephalopathy / Q000209:etiology; D006801:Humans; D006946:Hyperinsulinism / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D006975:Hypertension, Portal / Q000150:complications / Q000503:physiopathology / Q000628:therapy*; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance; D008103:Liver Cirrhosis / Q000150:complications / Q000503:physiopathology / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies
chemical_list: D007328:Insulin; D005947:Glucose